In the last few decades we have understood a major concept in the genesis of cardiac arrhythmia.Slowing in the propagation of cardiac impulse is a key trigger to precipitate a reentry circuit and initiate a tachy- arrhythmia.Still , many conditions like first degree AV block, chronic RBBB or even LBBB are benign entities as along as the heart is structurally normal .They seem never increase the incidence or life time risk of cardiac arrhythmia . Longevity is unaffected.( Or do we assume many things ?)

How is this possible ? or is the theory of slow conduction triggering reentry is flawed ?

Think again . . . if these patients who later on develop a structural heart disease , with an episode of ACS , myocardial or valvular disease, the original slow conduction substrates these people were harboring , will it become important ?

Surprisingly , we have no answers in literature.When Haissaguerre et al found preexisting ERS pattern could be a trigger for primary VF in case they develop ACS , he opened up a huge debate as it involved converting a vast number of normal population electrically anxious.

Now ,is it possible the so called benign blocks of heart like first degree AV blocks , RBBB , LAHBa , would be important at times of ACS and possibly make them prone for for primary ischemic arrhythmia .

Is bundle branch re-entry possible in structurally normal heart ?

We need answers. Some one , (Any EP fellow) somewhere could take up the issue and enlighten us !

LBBB is probably the most important conduction defect of the heart .When we say LBBB , we visualize a strikingly wide bizarre qrs complex .

Left bundle even though is considered a discrete structure , the fascicles make it a diffusely spread structure. Many varieties of LBBB with various degrees of involvement occur.

Talking about the basics of LBBB electrophysiology is out of place for the current generation cardiologists, who have little spare time as they sweat it out inside the cathlabs.

In early 1960s and 70s great articles came from pioneers regarding these defects. If we want get a good insight read this articles from Sodi palleres .Who says LBBB is a dynamic process, where it can occur from mild functional delay to a total block .

The conduction properties of left bundle is very much influenced by heart rate.

Law of statistics would suggest for every complete LBBB at least three to 4 times incidence of incomplete LBBB

Then . . .

Why we are not diagnosing ILBBB often ?

We miss it

Mistake it with LVH

We know it is there , but we do not want to diagnose it .

How to diagnose ILBBB?

See Sodi palleres criteria*

What is the relationship between qrs width and completeness of LBBB ?

Surprisingly and contrary to the belief , the width of the qrs has no linear correlation between severity of LBBB. In fact incomplete LBBB can occur with even 150ms qrs !

Then , what exactly determine the completeness of LBBB ?

What matters is , whether the down coming impulse gets blocked and split in the left side of the IVS or not ? This causes the the septal vector to change it’s direction ( ie right to left instead of the normal left to right) It removes the initial small r wave in v1 and q in v6 in complete LBBB. In incomplete LBBB these r and q are often retained .

My humble tributes to Barold, Sodi -palleres , and Leo Schamroth . Probably one of the best article on ILBBB is linked below. Reviewed in 1963 ! Not much data has been added in the next 47 years as on 2010

Ventricular tachycardia as a group , constitute a major group of cardiac arrhythmias. Most of the VTs are managed by cardioversion followed by medical management. Few require , implantable defibrillator when there is severe LV dysfucntion .(ICD) Localising the origin of VT and subsequent , ablation is the treatment of choice in some of the patients with VT.

Traditionally VT was thought to arise fro the endocardial aspects of myocardium. Now we realise many times VT originate from the epicardial aspects of ventricle.

Epicardial VT : Defintion

Epicardial ventricular tachycardia (VT) is defined as VT in which the critical sites of the reentrant circuit (or the ‘sites of origin’) are located exclusively in the subepicardial tissue, as shown by entrainment manoeuvres or VT that is terminated within 10 s with standard radiofrequency (RF) pulses, or both. E. SOSA,M. SCANAVACCA et all http://www.springerlink.com/content/w608142674154tp5/

This , gives us an idea that VT as an electrical abnormality has wide clinical presentations , life threatening at one end and, patient walking into the hospital with minimal palpitation on the other hand !

The management issues

In patients with hemodynamic instability , decision making is easy as there is only option of DC shock.

In patients with stable VT, it is natural for the physicians to get tentative or even confused.This is because , dangers of shocking a stable patient has to be weighed against the currently available excellent antiarrhytmic drugs( Amiodarone, Ibutilide etc) .

The major issue here is in ruling out underlying structural heart disease.

Never shock a stable VT, without knowing the myocardial and valvular function.There has been many occasions underlying severe LV dysfunction is missed and they may go for asystole.

VT in the setting of cardiomyopathy, Post MI(Scar mediated) are often refractory even to DC shocks.It is the drugs that will ultimately control the arrhythmia.DC shock is just used to terminate the VT.

VT structurally normal heart , especially arising the outflow tracts of LV or RV behave very differently (Fortunately they are more benign)

Have less hemodynamic impact as it involves the outflow tract and not over the the pumping zone of LV as in conventional ischemic myocardial VT .

They respond to calcium blockers verapamil to be precise (As they share properties of SVTs)

Sensitivity to verapamil by no way convey a meaning of Amiodarone resistance.Out flow tract VTs will also respond to Amiodarone many times.

Sinus node as the pacemaker , orchestrates the rhythm of life . It has to fire for the entire life time of a person.It can not afford to take any rest ! But it can pause a little bit , of course that pause could be less than 15% of it’s basic sinus length. This variation of sinus cycle length is called sinus arrhythmia.This is physiological. When it exceeds 15 % of the previous sinus cycle it is referred to as sinus pause.

Have a look at this ECG

What follows a long pause ?

By strict terms of definition a sinus pause should be followed by a delayed , next sinus beat only. A sinus pause , many times is followed by JPD – Junctional escape beat.This situation should be ideally referred to sinus arrest as the sinus node is taking too much of rest and it is not able to wake up from the slumber and it needs assistance form the junctional pace maker.

So even though sinus pause and sinus arrest is used many times interchangeably, it should be avoided.

What are the electrophysiological mechanisms of sinus pause ?

Simple sinus bradycardia . The commonest mechanism is the increased vagal tone. This occurs more often in young athletes. Eventhough increased vagal tone conveys a innocuous meaning , at times this can also be symptomatic and require intervention.

Sinus node exit block.

First degree, second degree, complete SA block can occur as in AV node.

First degree SA block can not be diagnosed by surface ECG. Third degree SA block is same as sinus arrest and subsidiary pacemaker will function in these patients. Second degree SA block is usually diagnosed when the sinus pause is in the multiples of resting sinus cycles. If the pauses are not in exact multiples sinus arrest is diagnosed. All these arrhythmia’s are collectively called sinus node dysfunction(SND)

How do you manage these patients?

Sinus node disorders can occur in number of systemic diseases*. It needs to be ruled out.

Infiltrating diseases like amyloidosis, hypothyroid states can result in SND.

Drug induced SND like beta blocker and calcium blockers are fairly common and should be excluded

Sinus node disorders are very often related to degenerative atrial diseases associated with HT, cardiomyopathy etc

*The list is not exhaustive

A very important association is noted with atrial fibrillation as a part of tachy brady syndrome .The link between SND and AF is obvious as atrial pathology is the common denominator in both ! This will be discussed later.

When is a pause significant ?

Any pause that is producing significant symptoms is significant.This depends upon the overall hemodynamic compensation of the patient.Young, and fit can even tolerate three second pause without symptoms.Underlying heart disease makes even a smaller pause symptomatic.But generally a 3 second or more pause is almost always pathological .Pauses can be up to 5 seconds ( a 5 second pause actually means a heart rate of 12/mt , obviously it can not go on for a minute, a patient will develop a syncope). A 3 second pause corresponds to 20/minute.

How will you evaluate a patient with sinus pause ?

There are sophisticated electrophysiological studies (EP) available like sinus node ECG ,sinus node function studies like sinus node recovery time, activation time etc. But these are generally of academic interest.

If a patient is symptomatic (syncope) because of bradycardia he requires a pacemaker and EP study is redundant . Similarly , if he is totally asymptomatic in spite of pauses , again EP study is not indicated.

Only for patients in the grey zone, further studies are indicated .This would include a extended holter, loop recorders, event monitors etc.

Another important issue to consider is , before putting a pacemaker patient”s symptom must be correlated with their arrhythmia.

What is the overlap between sinus node dysfunction and neuro cardiogenic syncope ?

SND can occur as an overlapping syndrome with neurocardiogenic syncope.(NCS ).NCS is also a very common cause of syncope .In NCS there are two limbs .Cardio inhibitory and vasodepressive. The cardio inhibitory form can exactly mimic an SND. In a given patient it is very difficult to pinpoint which of this limb is dominant.Head up tilt test(HUT) might help in few. If a patent’s symptoms are due to inappropriate vasodilatation pace maker may not reduce the symptom of dizziness or syncope.

Management

There is no ideal medical therapy* available as on date

Withholding all drugs which might aggravate bradycardia is of paramount importance.

Pace maker is the specific treatment in all symptomatic patients.

*Aminophyline tablet may be useful in some patients .It acts by antagonising adnosine receptors in SA node.Other drugs which can incrase the heart rate in the short term include Orcipranaline(Beta 2 stimulant /Alupent ) Probantheline(M 1 blocker)

The key issue is to avoid unnecessary pacemaker implants in patients who have insignificant pause.

Which pacemaker is ideal in SND ?

The need for dual or single chamber pacemker will be taken by the electrophysiologist .Atrial based pacemaker (AAI) is preferred as it gives physiological pacing .But a simple ventricle based VVI pace maker is good enough in vast majority of patients. This takes care of future risk of AV block also. DDD pace maker is the most physiological pacemaker and it is supposed to provide better quality of life. But it has an issue of insertion and maintenance of two leads, multi parameters to be programmed.It should switch to appropriate modes at different times.(Like VVI mode during atrial fibrillation etc).Trouble shooting needs expertise , while VVI is simple, safe , and just effective as well .(In this turbulent world, quality of life is a too trivial an issue to be determined by a DDD maker)

CRT , cardiac resynchronisation therapy is being projected as a revolutionary treatment for cardiac failure , where a failing heart is rewired electrically through multiple leads and make it contract more effectively.The success rate of CRT was highly variable.The basic question here is, there should be a significant documentation of desynchronisation prior to CRT , for resynchronisation to be effective. Further , the sites of myocardial stimulation ( Coronary sinus/LV epicardial) , dose of electricity and the sequence of stimulation and the electrical delay are very critical. Achieving this into perfection is not a simple job and is real rocket science ! ( If we can achieve 5 % of what the normal purkinje network do within the LV we can term it a huge success.) Let us hope we catch up with nature . Finally , it is ironical the sites of LV pacing , electrophysiologists select currently is infact not selected by them but pre selected by the patients coronary venous anatomy ! .So as on date , one can imagine how scientific this treatment could be !

Initially it was adviced for patients with only wide qrs later for even normal qrs patients.When people started using it indiscriminately insurance companies started to rethink and thus came the RETHINQ study in NEJM and brought a full stop to CRT in normal qrs CHF.

How to identify who will benefit from the costly CRT ?

It is a million dollar question. So millions of dollars were spent to identify the correct tool to identify the true responders to CRT.Echo cardiography with sophisticated methods tissue doppler, tissue tracking and , 3 D echo ,velocity vector imaging were done .These methods are not only costly but also time consuming and hugely expertise driven.